Chronic kidney disease (CKD) disturbs mineral homeostasis, leading to mineral and bone disorders (MBD). CKD‐MBD is a significant problem and currently available treatment options have important limitations. Phosphate retention is thought to be the initial cause of CKD‐MBD but serum phosphate remains normal until the late stages of CKD, due to elevated levels of the phosphaturic hormone fibroblast growth factor‐23 (FGF‐23), and parathyroid hormone (PTH). Reduction of 1,25‐dihydroxy‐vitamin D (1,25[OH]₂D) concentration is the next event in the adaptive response of the homeostatic system. We argue, and provide the rationale, that calcium retention which takes place concurrently with phosphate retention, could be the reason behind the hysteresis in the response of PTH. If indeed this is the case, intermittent administration of PTH in early CKD could prevent the hysteresis, which arguably leads to the development of secondary hyperparathyroidism, and provide the platform for an effective management of CKD‐MBD.